Chronic exposure to contaminated drinking water stimulates PPAR expression in mice livers

Mice were fed with source water (SW) and tap water (TW) for 90 d to evaluate hepatotoxicity induced by the drinking water. Histopathologic observation showed no obvious damage to hepatic tissue in the SW and TW groups. However, microarray analysis indicated that the SW and TW exposures affected many metabolic pathways, among which PPAR (peroxisome proliferator-activated receptors) signaling was most susceptible. Immunohistochemical staining demonstrated that both PPAR-α and PPAR-γ were significantly increased in the exposure groups compared to control. Enzyme-linked immunosorbent assay revealed that PPAR-α expression level was increased from 23.37 ± 0.53 ng g−1 liver weight in control group to 26.60 ± 1.43 ng g−1 liver weight in SW group and 27.68 ± 1.10 ng g−1 liver weight in TW group (p < 0.05). For PPAR-γ, the expression level was also significantly enhanced from 0.83 ± 0.07 ng g−1 liver weight in control group to 1.11 ± 0.20 ng g−1 liver weight in SW group and 1.16 ± 0.07 ng g−1 liver weight in TW group (p < 0.05). The SW and DW posed no obvious hepatotoxicity on mice and PPAR-α/-γ could be used as a novel biomarker to assess public health risk induced by slightly contaminated drinking water.

► Microarray detection of genomic toxicities induced by drinking water.
► Alteration of PPAR pathway by exposure to environmental water.
► Activation of PPAR-α/-γ by organic pollutants in drinking water.
► Use of PPAR-α/-γ as potential biomarker to assess public health risk.